New Research Collaboration Targets Role of CCL24 Protein in SSc

Patricia Inácio, PhD avatar

by Patricia Inácio, PhD |

Share this article:

Share article via email

Chemomab Therapeutics is teaming up with the University of Leeds to investigate the role of the protein CCL24 in scleroderma (SSc) — particularly how it contributes to blood vessel damage.

Their findings may aid in the clinical development of CM-101, Chemomab’s first-in-class antibody designed to target and neutralize CCL24.

A Phase 2 trial to test CM-101 in people with scleroderma, also known as systemic sclerosis, is planned to start early next year, Chemomab said in a press release announcing the collaboration.

The new research collaboration is led by Francesco Del Galdo, MD, PhD, an expert in the study of SSc and other rheumatic conditions, and head of the scleroderma program at the Leeds Musculoskeletal Biomedical Research Centre.

“We are delighted to partner with Prof. Del Galdo and his team to further study how CCL24 contributes to the vascular damage in SSc,” said Adi Mor, PhD, CEO of Chemomab. “They have developed state-of-the art models of vascular damage based on their large collection of SSc patient samples.”

Recommended Reading
preclinical study

Blocking Specific ‘Signaling Molecule’ Seen to Ease Inflammation, Scarring in Early Study

CCL24 is a type of molecule called a chemokine, which acts as a chemical attractant to immune cells, regulating cell trafficking, the formation of new blood vessels, and the production of collagen, which accumulates as fibrosis (scarring).

Notably, chemokines also have been suggested to promote the activation of fibroblasts into myofibroblasts — the cells responsible for the synthesis and buildup of scar tissue — a key process in scleroderma. These molecules also contribute to the activation of inflammatory cells, and impair blood vessel formation, also key in developing scleroderma.

Data from Chemomab and its collaborators have shown that levels of CCL24 are elevated in blood and skin samples of patients with scleroderma.

Using a mouse model of the condition, treatment with CM-101 was shown to lessen fibrosis (scarring) in the skin and lung, with further analyses demonstrating that the experimental medicine decreased the transition of fibroblasts into damaging myofibroblasts after being exposed to blood serum from SSc patients.

Also, according to Chemomab, CM-101 was safe and well-tolerated when given at different doses and multiple times in healthy people and in patients with nonalcoholic fatty liver disease.

“At Chemomab, we have extensively studied how CCL24 causes fibrosis and inflammation in preclinical SSc models,” Mor said.

“This collaboration is expected to increase our understanding of the association between CCL24 and vascular damage using human samples, with the aim of helping guide future SSc registration trials and ultimately providing benefit to these patients who have no effective treatment options,” she said.

Del Galdo noted that “extensive preclinical studies indicate that CCL24 is an important mediator of fibrosis and inflammation.”

“We welcome the opportunity to partner with Chemomab to better understand the role of CCL24 in causing the vascular damage that contributes significantly to the overall morbidity and mortality of SSc patients,” he said.